Abnormalities of the Cardiovascular System in Animals 

Based on the sources provided, the mechanisms leading to abnormalities of the cardiovascular system in animals can be detailed in a mind map format as follows:

Abnormalities of the Cardiovascular System in Animals (Mechanisms)

• 1. The cardiac valves fail to close or open properly (valvular disease)
  
  

  • Inadequate closure (coaptation) of valves leads to regurgitation (back flow of blood).

    • Most common form is mitral regurgitation, often with concurrent tricuspid regurgitation (~30% of cases with mitral regurgitation).

      • Primarily caused by myxomatous degeneration of the valve leaflets (degenerative mitral valve disease, DMVD).

        • DMVD is characterized by deposition and infiltration with glycosaminoglycans, disorganization and destruction of collagen and elastin within the extracellular matrix, and a lack of inflammation in valve tissue.

        • DMVD constitutes >75% of all heart disease in dogs.

        • It is most common in older small-breed dogs and older horses.

        • Cavalier King Charles Spaniels are affected more often and at a younger age than other breeds. It affects roughly 10% of dogs 5–8 years old, 20%–25% of those 9–12 years old, and 30%–35% of dogs older than 13 years.

      • Regurgitation through mitral or tricuspid valves results in an excessive amount of blood moving back and forth between the ventricle and atrium.

      • With mitral regurgitation, it is common to see dilation of the left atrium and left ventricle. The degree of left atrial enlargement may predict disease severity.

      • A typical holosystolic murmur is heard between the first and second heart sounds. A mid-systolic click may precede the murmur in early stages.

      • The intensity of the left apical systolic murmur in dogs with DMVD correlates well with the degree of mitral regurgitation. This correlation does not hold true in the face of systolic dysfunction or for myocardial disease, nor can it be applied to cats. Murmurs are graded on a scale of I–VI.

    • Less common is aortic regurgitation.

      • Occurs most often in older horses due to calcification or noninflammatory degeneration of the aortic valve.

      • May also develop secondary to aortic endocarditis, most often in large-breed dogs.

      • The left ventricle and atrium can become dilated proportional to the degree of regurgitation.

      • The murmur is always a diastolic murmur, heard immediately after the second heart sound. In horses, it can be "blowing" or "buzzing".

  • Inadequate opening of valves is termed stenosis.

    • Pulmonary valve stenosis is most prevalent.

    • Valvular aortic stenosis is uncommon, and mitral or tricuspid stenosis is rare.

    • Subaortic stenosis is prevalent, especially in certain breeds (Newfoundlands, Golden Retrievers, Boxers, Rottweilers, and German Shepherds).

      • Caused by a fibrous or fibromuscular band of tissue just beneath the aortic valve leaflets.

    • If a valve opens inadequately, a greater pressure must be generated to maintain normal blood flow.

    • The ventricle responsible for pumping blood through the stenotic valve concentrically hypertrophies (thickens) proportionally to the degree of tightness of the stenosis.

    • Systolic ejection quality murmurs are produced, heard between the first and second heart sounds. They are typically shorter than the holosystolic murmur of mitral regurgitation. They are heard best over the left heart base and thoracic inlet (subaortic stenosis).

    • In general, a louder murmur suggests greater stenosis, but intensity does not always predict severity. The velocity of blood flow through stenosis correlates with severity and can be estimated by spectral Doppler echocardiography or pressure gradient with cardiac catheterization.

    • Medications (beta-blockers) or interventional procedures (balloon valvuloplasty, stent/conduit for pulmonary stenosis) may be recommended in severe cases.

• 2. The heart muscle pumps inefficiently or relaxes inadequately (myocardial disease)
  
  

  • Impaired force of contraction is termed reduced systolic function (pump failure) or systolic dysfunction.

    • Occurs most commonly with dilated cardiomyopathy (DCM).

      • Includes primary idiopathic DCM in large- or giant-breed dogs (Dobermans, Great Danes, Irish Wolfhounds, etc.).

      • Includes DCM-phenotype with Boxer cardiomyopathy (arrhythmogenic right ventricular cardiomyopathy).

      • Seen in cats that are typically taurine deficient or in the end-stages of other cardiomyopathies.

      • Can occur in longstanding mitral regurgitation.

      • Can be associated with some grain-free diets, tachycardia-induced cardiomyopathy, doxorubicin-induced cardiomyopathy, and myocarditis.

      • When this occurs, the cardiac muscle is in a reduced inotropic state or has reduced contractile function.

      • In large-breed dogs, idiopathic DCM means the origin is unknown.

  • Impaired ventricular relaxation is termed reduced or impaired diastolic function.

    • Occurs most commonly when the cardiac muscle suffers oxygen debt and lacks energy for relaxation.

    • Seen as most cardiac diseases progress to heart failure.

    • Prominent in hypertrophic cardiomyopathy (HCM).

      • The muscle is too thick, stiff, and noncompliant, making ventricular filling poor.

      • HCM is the most common heart disease in cats (>85% of cats with heart disease).

    • Also seen in restrictive cardiomyopathy (stiffer walls, poor filling - small number of cats), nonspecific cardiomyopathy, or with pericardial disease.

      • Pericardial disease (thickened pericardium or fluid) interferes with diastolic function. It is most common in older, large-breed dogs with tumors bleeding into the pericardial sac (eg, hemangiosarcoma or chemodectoma).

• 3. The heart beats too slowly, too rapidly, or irregularly (arrhythmia)
  
  

  • Any cardiac rhythm outside the normal sinus rhythm is an arrhythmia.

  • They develop secondary to underlying structural heart disease, abnormalities of electrical pathways, or extracardiac causes.

  • An arrhythmia that is too fast, too slow, or too irregular can result in reduced cardiac output, causing clinical signs like exercise intolerance, syncope, or exacerbation of CHF.

  • Common types include:

    • Atrial fibrillation: Rapid, irregular rate. Seen commonly in horses and giant-breed dogs, or any size dog with advanced cardiac disease and severe left atrial enlargement. Depolarization of the atria is not coordinated, stimulation of the AV node is frequent but random. Results in an irregularly irregular rhythm with absence of P waves on ECG.

    • Ventricular premature depolarizations (VPDs/VPBs): Arise from regions of electrical instability in the ventricles. Commonly results from chronic stretch of fibers, fibrosis or fibrofatty infiltration, oxygen debt (ischemia or hypoxia), or drug effects. Seen most commonly in Boxers and Doberman Pinschers (dogs that develop ARVC or DCM). A single beat typically does not cause clinical signs and can be benign. Premature beats may evolve into bursts (ventricular tachycardia) or long runs, leading to hemodynamic impairment and syncope, or even ventricular fibrillation and sudden death. Ventricular tachycardia commonly occurs in Doberman Pinschers with DCM and Boxers or Bulldogs with ARVC and warrants immediate treatment.

    • Sick sinus syndrome: Transient arrest of SA node discharge alternating with periods of tachycardia. Seen mainly in aged Miniature Schnauzers, Pugs, and West Highland White Terriers. The ventricular rate is exceptionally slow during arrest and may lead to hemodynamic impairment, exercise intolerance, syncope, or sudden death. A pacemaker is indicated if symptomatic.

    • Persistent atrial standstill: Seen in Labrador Retrievers and English Springer Spaniels. Pacemaker indicated if persistent.

    • Third-degree AV block (complete heart block): No atrial depolarization enters the ventricles. Seen in older dogs with AV nodal fibrosis. The ventricular rate is exceptionally slow and may lead to hemodynamic impairment, exercise intolerance, syncope, or sudden death. A pacemaker is indicated for persistent high-grade block.

• 4. The systemic vessels offer too great an interference to blood flow (vascular disease)
  
  

  • Primarily involves interference to blood flow through systemic arterioles, resulting in systemic hypertension.

  • Most common in aging animals with impaired renal function (dogs and cats), hyperadrenocorticism (dogs), or hyperthyroidism (cats).

  • The exact underlying cause is usually unknown. Suspected causes include sodium retention and plasma volume expansion, hyperaldosteronism, increased sympathetic tone, and possibly increased angiotensin II.

  • A loss in arteriolar compliance may persist even with adequate treatment of the associated clinical condition.

  • Arterial vasodilators, such as ACE inhibitors and amlodipine, are a mainstay of antihypertensive therapy. ACVIM consensus statement exists for diagnosis and management.

• 5. Abnormal communications between chambers or circulations (cardiac shunts, extracardiac shunts)
  
  

  • Termed cardiovascular shunts, these are abnormal communications between the left and right side of the circulation.

  • Types in decreasing prevalence: patent ductus arteriosus (between aorta and pulmonary trunk), ventricular septal defect (between left and right ventricles), or atrial septal defect (between left and right atria).

  • Most commonly, blood crosses from the left side to the right side (termed left-to-right shunts).

    • Result in overcirculation of the lungs and dilatation of the cardiac chambers involved in pumping or carrying the shunted blood.

    • Chronic dilatation may ultimately lead to myocardial failure.

  • Less commonly, blood crosses from the right side to the left side (right-to-left shunts).

    • Allows poorly oxygenated blood into the systemic circulation.

    • Causes a bluish tinge to mucous membranes (cyanosis) and increased numbers of RBCs (polycythemia).

    • Tetralogy of Fallot is a complex congenital anomaly (hypoplastic RV outflow/pulmonary stenosis, overriding aorta, VSD, RV hypertrophy) and is the most common form of a right-to-left shunt.

    • Any large atrial or ventricular septal defect can result in right-to-left shunting (Eisenmenger physiology) secondary to pulmonary hypertension from chronic pulmonary overcirculation. Right-to-left shunting PDA also occurs, typically from persistent pulmonary hypertension from birth.

    • Any shunt can originate as left-to-right and reverse direction if pressure within the pulmonary circulation or right heart becomes greater than the pressure in the aorta or left heart.

• 6. There is too little or too much blood compared with the ability of the blood vessels to store that blood.
  
  

  • The provided sources list this mechanism but do not elaborate further on the specific conditions or pathophysiology associated with it.

• 7. There is parasitism of the cardiovascular system (eg, heartworm disease)
  
  

  • Refers primarily to heartworm disease.

  • Transmitted via mosquitoes.

  • Seen predominantly in dogs but also in cats.

  • Adult heartworms in the pulmonary vessels, and the pulmonary arterial changes they induce, impede flow through the lungs.

  • This can induce severe, persistent pulmonary hypertension.

  • Leads to right ventricular hypertrophy, increased right-side filling pressure, and eventual development of right-side CHF (cor pulmonale).

  • The disease progresses at varying rates in dogs but usually lasts < 2 yr in cats.

  • Animals may develop syncope or cor pulmonale from pulmonary hypertension.

  • Pulmonary thromboembolism can occur from in situ thrombus formation or adult worm death.

  • Antigenic stimulation from heartworms may cause eosinophilic pneumonitis.

  • The death of adult worms secondary to adulticide therapy always results in some degree of pulmonary thromboembolism. Strict cage rest is necessary after adulticide therapy. Pretreatment with doxycycline and ivermectin may mitigate pulmonary pathology from worm death.

These mechanisms lead to common endpoints of heart disease. Signs are due either to inadequate organ perfusion (low output, or forward heart failure), causing exercise intolerance, weakness, syncope, or azotemia, or to blood damming up in organs (congestive heart failure, CHF), causing effusions or organ edema/malfunction. Cyanosis and polycythemia can result from inadequate oxygenation. Heart failure involves a complex interaction between a failing heart (affected by one or more of these mechanisms) and the blood vessels.